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BACKGROUND AND AIMS: Systemic inflammatory diseases could act as an unfavorable condition in which epicardial adipose tissue (EAT) becomes harmful to cardiovascular health. The objectives were: (a) to quantitatively compare the presence of EAT between patients with systemic inflammatory diseases and controls; (b) to analyze the association between EAT and subclinical atheromatosis in individuals with systemic inflammatory diseases. METHODS: Studies that have quantified EAT in a population with systemic inflammatory diseases compared to a control group, or that describe the association between EAT and the presence of subclinical atheromatosis in patients with systemic inflammatory diseases were included. A quantitative analysis was performed for the first objective. This systematic review was performed according to PRISMA guidelines. RESULTS: Twenty-one studies including 1448 patients with systemic inflammatory diseases, were considered eligible for this study. Patients with systemic inflammatory disease have a higher volume (MD: 10.4cm3 [1.8-19.1]; p<0.01), higher thickness (MD: 1.0mm [0.8-1.2]; p<0.01), and a statistically non-significant higher area (MD: 3.1cm2 [1.0-5.2]; p=0.46) of EAT compared to the control group. Most studies reported a significant association between EAT and subclinical atheromatosis in patients with different systemic inflammatory diseases. CONCLUSION: This study demonstrated that EAT is increased in patients with systemic inflammatory diseases compared with healthy controls, and that EAT measurement is closely correlated with subclinical atherosclerosis in these patients. The causality of this association should be tested in prospective studies.

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Abstract Background: Inflammation, which is associated with an unhealthy lifestyle, plays a critical role in the development of both cardiometabolic diseases (CMD) and cancer. Carcinoembryonic antigen (CEA) is a tumor marker which also has proinflammatory properties. Recent studies have reported CEA to be associated with atherosclerosis, metabolic syndrome, and visceral adiposity. Epicardial adipose tissue (EAT) can exhibit highly inflammatory and pathogenic properties, and is a known risk factor for CMD. However, its relationship with CEA is still unknown. Objectives: This study aimed to investigate the possible association of CEA with EAT. Methods: A total of 134 Caucasian (males = 56, females = 78) individuals, aged (22-83 years), who were admitted for routine health control, were enrolled in this cross-sectional study. CEA was measured with chemiluminescent microparticle immunoassay (CMIA). EAT was measured by transthoracic echocardiography, and the visceral fat rating (VFR) was assessed by a body composition analyzing machine. The p-value <0.05 was considered statistically significant. Results: CEA levels were categorized as tertiles: T1, 0.5-1.04; T2, 1.06-1.69; and T3, ≥1.7 ng/ml. The mean age, weight, VFR, EAT, and fasting glucose, as well as the median of systolic blood pressure (SBP), creatinine, and AST increased with the increasing CEA tertiles. CEA was significantly associated with EAT (r = 0.55, P<0.001) and VFR (r = 0.36, P<0.001). Multivariate linear regression analysis confirmed that gender, age, and EAT were the significant independent variables associated with CEA. Conclusion: Individuals with increased EAT have higher levels of CEA, suggesting that this biomarker is most likely produced by EAT; however, additional investigations are required to improve the present work.

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Objective: To evaluate the expression of UCP1, UCP2, and UCP3 mRNA and encoded proteins in epicardial and mediastinal adipose tissues in patients with coronary artery disease (CAD). Subjects and methods: We studied 60 patients with CAD and 106 patients undergoing valve replacement surgery (controls). Expression levels of UCP1, UCP2, and UCP3 mRNA and encoded proteins were measured by quantitative real-time PCR and Western blot analysis, respectively. Results: : We found increased UCP1, UCP2, and UCP3 mRNA levels in the epicardial adipose tissue in the CAD versus the control group, and higher UCP1 and UCP3 mRNA expression in the epicardial compared with the mediastinal tissue in the CAD group. There was also increased expression of UCP1 protein in the epicardial tissue and UCP2 protein in the mediastinum tissue in patients with CAD. Finally, UCP1 expression was associated with levels of fasting plasma glucose, and UCP3 expression was associated with levels of high-density lipoprotein cholesterol and low-density cholesterol in the epicardial tissue. Conclusion: Our study supports the hypothesis that higher mRNA expression by UCP genes in the epicardial adipose tissue could be a protective mechanism against the production of reactive oxygen species and may guard the myocardium against damage. Thus, UCP levels are essential to maintain the adaptive phase of cardiac injury in the presence of metabolic disorders.

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Several small studies have evaluated the association between epicardial adipose tissue (EAT) and pregnancy-related cardiovascular risk factors such as gestational diabetes mellitus (GDM) or hypertensive disorders. The objective of this study was to quantitatively compare EAT thickening between patients with GDM or pregnancy-related hypertensive disorders and healthy controls. This systematic review and meta-analysis were performed according to PRISMA guidelines. A literature search was performed to detect studies that have quantified EAT in women with GDM and pregnancy-related hypertensive disorders compared to a control group. The primary outcome was EAT thickening estimated by ultrasound expressed in millimeters. Random or fixed effects models were used. Nine observational studies including 3146 patients were identified and considered eligible for this systematic review. The quantitative analysis showed that patients with GDM have a higher EAT thickness (mean difference: 1.1 mm [95% confidence interval: 1.0-1.2]; I2 = 24%) compared to the control group. Moreover, patients with pregnancy-related hypertensive disorders showed higher EAT thickness (mean difference: 1.0 mm [95% confidence interval: 0.6-1.4]; I2 = 83%) compared to the control group. In conclusion, this study demonstrated that EAT thickening is increased in patients with GDM and pregnancy-related hypertensive disorders compared with healthy controls. Whether or not this association is causal should be evaluated in prospective studies.

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ABSTRACT Objective: To evaluate the expression of UCP1, UCP2, and UCP3 mRNA and encoded proteins in epicardial and mediastinal adipose tissues in patients with coronary artery disease (CAD). Subjects and methods: We studied 60 patients with CAD and 106 patients undergoing valve replacement surgery (controls). Expression levels of UCP1, UCP2, and UCP3 mRNA and encoded proteins were measured by quantitative real-time PCR and Western blot analysis, respectively. Results: We found increased UCP1, UCP2, and UCP3 mRNA levels in the epicardial adipose tissue in the CAD versus the control group, and higher UCP1 and UCP3 mRNA expression in the epicardial compared with the mediastinal tissue in the CAD group. There was also increased expression of UCP1 protein in the epicardial tissue and UCP2 protein in the mediastinum tissue in patients with CAD. Finally, UCP1 expression was associated with levels of fasting plasma glucose, and UCP3 expression was associated with levels of high-density lipoprotein cholesterol and low-density cholesterol in the epicardial tissue. Conclusions: Our study supports the hypothesis that higher mRNA expression by UCP genes in the epicardial adipose tissue could be a protective mechanism against the production of reactive oxygen species and may guard the myocardium against damage. Thus, UCP levels are essential to maintain the adaptive phase of cardiac injury in the presence of metabolic disorders.

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RESUMEN La asociación entre el tejido adiposo visceral y la enfermedad cardiovascular ha sido claramente establecida. Asimismo, se ha determinado que la adiposidad ectópica se asocia con un mayor riesgo cardiovascular en comparación a la adiposidad subcutánea. En este contexto, múltiples investigaciones han evaluado el rol del tejido adiposo epicárdico (TAE) en la enfermedad cardiovascular. El TAE se localiza entre la superficie miocárdica y la hoja visceral del pericardio, y puede cuantificarse mediante técnicas no invasivas como ser el ecocardiograma, la tomografía computada o la resonancia nuclear magnética. El TAE no es simplemente un órgano de depósito. Actualmente, se considera que es un tejido metabólicamente activo capaz de secretar múltiples adipoquinas que actúan mediante diferentes vías de señalización parácrina, endócrina, vasócrina y/o autócrina. La evidencia actual sugiere que el TAE puede ser un factor contribuyente en la patogénesis de la enfermedad coronaria, asociándose además con su gravedad y progresión. En ese sentido, algunos autores han postulado al TAE como un nuevo factor de riesgo cardiovascular y como un potencial blanco terapéutico. El objetivo de esta revisión es analizar la relación del TAE con la enfermedad cardiovascular, principalmente con la enfermedad coronaria.

ABSTRACT The association between visceral adipose tissue and cardiovascular disease has been clearly established. Likewise, it has been determined that ectopic adiposity is associated with a higher cardiovascular risk compared to subcutaneous adiposity. In this context, multiple investigations have evaluated the role of epicardial adipose tissue (EAT) in cardiovascular disease. EAT is located between the myocardial surface and the visceral layer of the pericardium, and can be quantified by noninvasive techniques such as echocardiography, computed tomography, or magnetic resonance imaging. The EAT is not simply a storage organ. Currently, it is considered to be a metabolically active tissue capable of secreting multiple adipokines that act through different paracrine, endocrine, vasocrine and/or autocrine signaling pathways. Current evidence suggests that EAT may be a contributing factor in the pathogenesis of coronary heart disease, as well as being associated with its severity and progression. In this sense, some authors have postulated EAT as a new cardiovascular risk factor and as a potential therapeutic target. The aim of this review is to analyze the association between EAT and cardiovascular disease, mainly coronary artery disease.

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(1) Sodium-glucose cotransporter-2 inhibitors (SGLT2-i) reduce adipose tissue and cardiovascular events in patients with type 2 diabetes (T2D). Accumulation of epicardial adipose tissue (EAT) is associated with increased cardio-metabolic risks and obstructive coronary disease events in patients with T2D. (2) We performed a systematic review and meta-analysis of SGLT2-i therapy on T2D patients, reporting data on changes in EAT after searching the PubMed/MEDLINE, Embase, Science Direct, Scopus, Google Scholar, and Cochrane databases. A random effects or fixed effects model meta-analysis was then applied. (3) Results: A total of three studies (n = 64 patients with SGLT2-i, n = 62 with standard therapy) were included in the final analysis. SGLT2 inhibitors reduced EAT (SMD: -0.82 (-1.49; -0.15); p < 0.0001). An exploratory analysis showed that HbA1c was significantly reduced with SGLT2-i use, while body mass index was not significantly reduced with this drug. (4) Conclusions: This meta-analysis suggests that the amount of EAT is significantly reduced in T2D patients with SGLT2-i treatment.

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Epicardial adipose tissue (EAT) is correlated with endothelial dysfunction, metabolic syndrome, increased mortality and recent studies showed a possible association with the increased risk of stroke. We performed a systematic review of studies evaluating the association between EAT and stroke. Eighty studies met the inclusion criteria and were consequently analyzed. The review had Five main findings. First, the increased epicardial fat thickness (EFT) may be associated with the stroke episode. Second, regardless of the imaging method (echocardiography, MRI, and CT) this association remains. Third, the association of metabolic syndrome and atrial fibrillation seems to increase the risk of stroke. Fourth, this systematic review was considered as low risk of bias. Despite being unable to establish a clear association between EAT and stroke, we have organized and assessed all the research papers on this topic, analyzing their limitations, suggesting improvements in future pieces of research and pointing out gaps in the literature. Furthermore, the mechanistic links between increased EAT and stroke incidence remains unclear, thus, further research is warranted.

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According to previous epidemiological studies, we can reduce the thickness of epicardial fat and improve cardiovascular risk factors through exercise, and the changes may depend on the form of exercise. We systemically reviewed published studies that evaluated exercise intervention on epicardial adipose tissue (EAT) levels. We included randomized controlled trials (RCTs) comparing one exercise with another exercise or diet for the treatment to reduce EAT. We used fixed effects models for meta-analyses; effects of exercise on outcomes were described as mean differences (MD) or standardized difference of means (SMD) was used, their 95% confidence intervals (CI). Five RCTs were included (n = 299), 156 in exercise group and 143 in the control. In comparison to the control group, exercise significantly reduced EAT (SMD - 0.57, 95%CI - 0.97 to - 0.18) and waist circumference (MD - 2.95 cm, 95%CI - 4.93 to - 0.97). Exercise did not have an effect on BMI (MD - 0.23 kg/m2, 95%CI - 0.73 to 0.27), weight (MD - 0.06 kg, 95%CI - 1.46 to 1.34), or HDL (SMD 0.26, 95%CI - 0.06 to 0.57).VO2 was significantly increased by exercise (SMD 1.58, 95%CI 1.17 to 1.99). Risk of bias was high for 3 studies, and GRADE quality of evidence was very low to moderate. Exercise reduced epicardial adipose tissue and waist circumference, and did not have effect on weight, BMI, or HDL. Newer trials with better design and methods are necessary to improve the quality of the evidence. PROSPERO registration number (CRD42018096581).

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BACKGROUND: Coronary artery disease (CAD) is the leading cause of morbidity and mortality worldwide. Recently, triglyceride rich lipoproteins are proposed to contribute to CAD risk; its concentrations would be partly determined by lipoprotein lipase (LPL) and endothelial lipase (EL). Epicardial adipose tissue (EAT), a visceral AT surrounding myocardium and coronary arteries, emerged as an important actor in CAD; the increase in its volume could be a consequence of LPL and EL. Circulating enzymes levels would be conditioned by local tissue factors. Our aim was to evaluate LPL, EL and their regulators levels in serum and EAT from CAD patients, searching for possible parallelisms and their role in the lipoprotein profile. METHODS: In serum, EAT and subcutaneous AT (SAT) from patients undergoing coronary artery bypass graft (CABG, n = 25) or valve replacement (No CABG, n = 25), LPL, EL and glycosylphosphatidylinositol-anchored high density lipoprotein-binding protein-1 (GPIHBP1) expression were evaluated. Besides, Apoprotein (Apo)CII, CIII and AV were determined in serum, along with lipoprotein profile. RESULTS: Insulin-resistance markers were higher in CABG (p < 0.05). Serum LPL levels were decreased (p = 0.045), while EL levels increased (p < 0.001) in CABG, without differences in EAT or SAT. Circulating GPIHBP1 concentrations were decreased in CABG (p = 0.047), while EAT GPIHBP1 expression was increased (p < 0.001). ApoCII and ApoAV concentrations were higher in CABG (p = 0.016 and p = 0.047, respectively), without differences in ApoCIII concentrations between groups. CONCLUSIONS: In EAT, LPL and EL protein levels were not changed in CAD, although GPIHBP1 protein levels were higher. EAT would be a minor contributor to the circulating levels of the enzymes.

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